Rheumatoid arthritis (RA) and chronic periodontitis are the most common chronic inflammatory diseases with remarkable pathological and clinical similarities. A lot of similarities exist between RA and periodontitis at cellular and molecular levels. The relationship between these two chronic inflammatory diseases is still unclear. This case-control study was undertaken to determine the possible association between chronic inflammatory diseases like RA and periodontitis. The case group consisted of 100 patients attending the Rheumatology clinic who have rheumatoid arthritis (RA group). Age- and gender-matched 112 patients without RA attending the Outpatient wing of Department of General Medicine formed the control group (NRA group). The number of missing teeth, gingival index (GI), oral hygiene index-simplified (OHI-S), probing pocket depth (PPD) and clinical attachment levels (CAL) were evaluated in both the groups. Rheumatoid disease activity was assessed by DAS-28 score system. Systemic markers of inflammation like erythrocytic sedimentation rate (ESR) and serum levels of C-reactive protein (CRP) were assessed. There was a statistically significant difference in GI, OHI-S, PPD, CAL, ESR and CRP levels between cases (RA group) and controls (NRA group) (P < 0.05). Among subjects with RA, there was no association between the rheumatoid disease activity and the severity of periodontal disease. The occurrence and severity of periodontitis was found to be higher in RA subjects as compared to subjects without RA, suggesting a positive relation between these two chronic inflammatory diseases.
Whether to treat hyperuricemia uncomplicated by articular gout, urolithiasis, or uric acid nephropathy is an exercise in clinical judgment and universal agreement is lacking. Patients with coronary artery disease, chronic kidney disease, and early onset hypertension with persistent hyperuricemia are likely to be benefited with urate-lowering therapy. The paradigm of the causative association of hyperuricemia with cardiovascular and chronic kidney diseases seems to have progressed from skepticism to increasing evidence of a true relationship. Although such evidences are mounting, they are not enough to support pharmacotherapy for all patients with asymptomatic hyperuricemia. Further studies are needed to determine which patients are likely to get beneficial effects from pharmacotherapy and the minimum threshold of uric acid level required to experience clinical benefits.
Background: Gout is the most prevalent inflammatory arthritis in the Asia-Pacific region and worldwide. This clinical practice guideline (CPG) aims to provide recommendations based on systematically obtained evidence and values and preferences tailored to the unique needs of patients with gout and hyperuricemia in Asia, |LORENZO Et aL. | INTRODUC TI ONGout is the most prevalent inflammatory arthritis in the Asia-Pacific region and worldwide. 1 Its prevalence increased steadily in various countries: 2.7% in the 1990s to 3.9% in early 2000 in the United States and from 3.4 per 1000 in 2007 to 7.6 per 1000 persons in 2015 in Korea. 2,3 The prevalence is higher in certain ethnic groups.The risk for tophi formation tends to be higher after controlling for age, gender, hypertension, diuretic use, and kidney function. 4 Varying prevalence across ethnic groups indicates that genetics affects its development and the individual's risk when exposed to environmental or dietary variables. 5,6 Despite scientific advancements, disease control of gout is suboptimal. 2,3 Clinical practice guidelines (CPG) from Western and several Asian countries have provided recommendations for the management of gout. [7][8][9] However, the need to formulate unified Asia-Pacific recommendations was recognized. This CPG aims to provide evidence-based recommendations in managing gout in its different phases: asymptomatic hyperuricemia, acute gout, intercritical gout, and chronic tophaceous or complicated gout. It covers both pharmacologic and non-pharmacologic interventions (NPI) with consideration of the unique needs of patients with gout in Asia, Australasia, and the Middle East. The target users of these guidelines are general practitioners and specialists, including rheumatologists, in different clinical settings in these regions. | G UIDELINE DE VELOPMENT ME THODSThe Steering Committee (SC) formed the guideline development working groups (GDG), formulated the guideline questions (Table 1) in PICO (population, intervention, comparator, and outcome) format, and oversaw the CPG processes (Figure 1). The Technical Working Group (TWG) appraised and summarized the evidence, applied the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology to determine the certainty of evidence, and drafted the recommendations.The Consensus Panel (CP) was composed of 9 key stakeholders (rheumatologists, general practitioners, academicians, and a patient representative) from Australia,
Persistence of pain noted in post-CKG disease resulted in significantly deteriorated functional status of those affected.
Even though, Hippocrates recognized gout as an affection of older men and a product of high living long back in 5th century BC, this painful condition promises to accompany humanity to the 21st century. The incidence is progressively rising and females are also affected in the modern era. There are also regional and ethnic variations in the incidence, the genetics of which is being studied. The recommended best therapy for the acute attacks and long term prophylaxis has improved remarkably in the recent years. However, patients are often treated inadequately and risk factors for their disease are not well explored in daily practice. Although well designed long term studies of current and newer treatment are welcomed, educating doctors especially the primary care physicians who manage majority of gout cases, in optimizing the currently available management options would improve the present care.Key words: disease aetiology and pathogenesis -human, gout, metabolic and crystal arthropathies drug treatment, metabolic and crystal arthropathies epidemiology, metabolic and crystal arthropathies inflammasome.
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